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TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx.

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  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
      Calcium/*metabolism ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Neurons/*metabolism ; TRPM Cation Channels/*metabolism; Animals ; Calcium Signaling/drug effects ; Cell Line, Tumor ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors ; Isoquinolines/pharmacology ; Mice ; Neurons/drug effects ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/pharmacology ; Sulfonamides/pharmacology
    • Abstract:
      The nonspecific divalent cation channel TRPM7 (transient receptor potential-melastatin-like 7) is involved in many Ca2+ and Mg2+-dependent cellular processes, including survival, proliferation and migration. TRPM7 expression predicts metastasis and recurrence in breast cancer and several other cancers. In cultured cells, it can induce an invasive phenotype by promoting Ca2+-mediated epithelial-mesenchymal transition. We previously showed that in neuroblastoma cells that overexpress TRPM7 moderately, stimulation with Ca2+-mobilizing agonists leads to a characteristic sustained influx of Ca2+. Here we report that sustained influx through TRPM7 is abruptly abrogated by elevating intracellular levels of cyclic adenosine monophosphate (cAMP). Using pharmacological inhibitors and overexpression studies we show that this blockage is mediated by the cAMP effector Protein Kinase A (PKA). Mutational analysis demonstrates that the Serine residue S1269, which is present proximal to the coiled-coil domain within the protein c-terminus, is responsible for sensitivity to cAMP.
      Competing Interests: The authors have declared that no competing interests exist.
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    • Accession Number:
      0 (Isoquinolines)
      0 (Protein Kinase Inhibitors)
      0 (Sulfonamides)
      0 (TRPM Cation Channels)
      E0399OZS9N (Cyclic AMP)
      EC 2.7.1.- (Trpm7 protein, mouse)
      EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
      M876330O56 (N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide)
      SY7Q814VUP (Calcium)
    • Publication Date:
      Date Created: 20190108 Date Completed: 20190923 Latest Revision: 20200309
    • Publication Date:
      20250114
    • Accession Number:
      PMC6322742
    • Accession Number:
      10.1371/journal.pone.0209563
    • Accession Number:
      30615643